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dc.contributor.authorTumpara, Srinu
dc.contributor.authorBallmaier, Matthias
dc.contributor.authorWrenger, Sabine
dc.contributor.authorKönig, Mandy
dc.contributor.authorLehmann, Matthias
dc.contributor.authorLichtinghagen, Ralf
dc.contributor.authorMartinez-Delgado, Beatriz 
dc.contributor.authorKorenbaum, Elena
dc.contributor.authorDeLuca, David
dc.contributor.authorJedicke, Nils
dc.contributor.authorWelte, Tobias
dc.contributor.authorFromme, Malin
dc.contributor.authorStrnad, Pavel
dc.contributor.authorStolk, Jan
dc.contributor.authorJanciauskiene, Sabina
dc.date.accessioned2021-06-10T18:14:58Z
dc.date.available2021-06-10T18:14:58Z
dc.date.issued2021-05-18
dc.identifier.citationElife. 2021 May 18;10:e64881.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13127
dc.description.abstractThe CX3CR1 (chemokine (C-X3-C motif) receptor 1) expression levels on immune cells have significant importance in maintaining tissue homeostasis under physiological and pathological conditions. The factors implicated in the regulation of CX3CR1 and its specific ligand CX3CL1 (fractalkine) expression remain largely unknown. Recent studies provide evidence that host`s misfolded proteins occurring in the forms of polymers or amyloid fibrils can regulate CX3CR1 expression. Herein, a novel example demonstrates that polymers of human ZZ alpha-1 antitrypsin (Z-AAT) protein, resulting from its conformational misfolding due to the Z (Glu342Lys) mutation in SERPINA1 gene, strongly lower CX3CR1 mRNA expression in human PBMCs. This parallels with increase of intracellular levels of CX3CR1 and Z-AAT proteins. Presented data indicate the involvement of the CX3CR1 pathway in the Z-AAT-related disorders and further support the role of misfolded proteins in CX3CR1 regulation.es_ES
dc.description.sponsorshipFunder: Deutsche Forschungsge-meinschaft, Grant number: STR 1095/6-1, Author: Pavel Strnad. Funder: Deutsche Zentrum für Lungen-forschung, Grant number: 82DZL002A, Author: Sabina Janciauskiene. Funder: Deutsche Forschungsge-meinschaft, Grant number: SFB/TRR57, Author: Pavel Strnad. The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.es_ES
dc.language.isoenges_ES
dc.publishereLife Sciences Publications es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCell biologyes_ES
dc.subjectHumanes_ES
dc.subjectMedicinees_ES
dc.titlePolymerization of misfolded Z alpha-1antitrypin protein lowers CX3CR1 expression in human PBMCses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID34002692es_ES
dc.format.volume10es_ES
dc.format.pagee64881es_ES
dc.identifier.doi10.7554/eLife.64881es_ES
dc.contributor.funderDeutsche Forschungsgemeinschaft (Alemania) es_ES
dc.contributor.funderGerman Center for Lung Research (Alemania) es_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn2050-084Xes_ES
dc.relation.publisherversionhttps://doi.org/10.7554/eLife.64881es_ES
dc.identifier.journalELifees_ES
dc.repisalud.centroISCIII::Instituto de Investigación de Enfermedades Rarases_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
This item is licensed under a: Atribución 4.0 Internacional